1. Field of the Invention
The present invention relates generally to medical devices; and more particularly to an implantable cardiac stimulator that provides a hierarchical approach to the treatment of ventricular arrhythmias, utilizing combinations of pacing, cardioverting, and defibrillating therapies.
2. Relevant Background
In the normal human heart, the sinus node generally located near the junction of the superior vena cava and the right atrium constitutes the primary natural pacemaker by which rhythmic electrical excitation is developed. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, or atria, at the right and left sides of the heart. In response to this excitation, the atria contract, pumping blood from those chambers into the respective ventricular chambers, or ventricles. The impulse is transmitted to the ventricles through the atrioventricular (A-V) node, or junction, and via a conduction system comprising the bundle of His, or common bundle, the right and left bundle branches, and the Purkinje fibers. In response, the ventricles contract, the right ventricle pumping unoxygenated blood through the pulmonary artery to the lungs and the left ventricle pumping oxygenated (arterial) blood through the aorta and the lesser arteries to the body. The right atrium receives the venous (unoxygenated) blood from the upper part of the body (head, neck and chest) via the superior vena cava, or upper great vein, and from the lower part of the body (abdomen and legs) via the inferior vena cava, or lower great vein. The blood oxygenated by the lungs is carried via the pulmonary veins to the left atrium.
This action is repeated in a rhythmic cardiac cycle in which the atrial and ventricular chambers alternately contract and pump, then relax and fill. One-way valves along the veins, between the atrial and ventricular chambers in the right and left sides of the heart (the tricuspid valve and the mitral valve, respectively), and at the exits of the right and left ventricles (the pulmonary and aortic valves, respectively) prevent backflow of the blood as it moves through the heart and the circulatory system.
The sinus node is spontaneously rhythmic, and the cardiac rhythm originating from that primary natural pacemaker is termed sinus rhythm. This capacity to produce spontaneous cardiac impulses is called rhythmicity, or automaticity. Some other cardiac tissues possess this electrophysiologic property and hence constitute secondary natural pacemakers, but the sinus node is the primary pacemaker because it has the fastest spontaneous rate. The secondary pacemakers tend to be inhibited by the more rapid rate at which impulses are generated by the sinus node.
The resting rates at which sinus rhythm occurs in normal persons differ from age group to age group, generally ranging between 110 and 150 beats per minute ("bpm") at birth, and gradually slowing in childhood to the range between 65 and 85 bpm usually found in adults. The resting sinus rate (hereinafter termed simply the "sinus rate") varies from one person to another, and despite the aforementioned usual adult range, is generally considered to lie anywhere between 60 and 100 bpm (the "sinus rate range") for the adult population.
A number of factors may affect the rate of sinus rhythm within the sinus rate range, and some of those factors may slow or accelerate the rate sufficiently to take it outside the sinus rate range. The slower rates (below 60 bpm) are called sinus bradycardia, and the higher rates are termed sinus tachycardia. In particular, sinus tachycardia observed in healthy persons arises from various factors which may include physical or emotional stress (exercise or excitement), consumption of beverages containing alcohol or caffeine, cigarette smoking, and ingestion of certain drugs. The sinus tachycardia rate usually ranges between 101 and 160 bpm in adults, but has been observed at rates up to (and in infrequent instances, exceeding) 200 bpm in younger persons during strenuous exercise.
Sinus tachycardia is sometimes categorized as a cardiac arrhythmia, since it is a variation from normal sinus rate range. Arrhythmia rates which exceed the upper end of the sinus rate range are termed tachyarrhythmias. Healthy persons usually experience a gradual return to the sinus rate after removal of the factor(s) giving rise to sinus tachycardia, and hence, treatment of the arrhythmia is not necessary unless it is found to be attributable to disease. Abnormal arrhythmias (which are hereinafter simply termed "arrhythmias", and in the case of abnormal tachyarrhythmias, simply termed "tachyarrhythmias", to mean arrhythmias associated with cardiac or other disease, and which are to be contrasted with arrhythmias not associated with disease and for which the modifier "normal" will hereinafter sometimes be used), however, may require special treatment, and in some instances require immediate emergency treatment toward preventing sudden death of the afflicted individual.
It is a principal object of the present invention to provide an improved medical device for treating arrhythmias, which employs a hierarchical approach to such treatment.
The electrophysiologic properties of the heart include excitability and conductivity, as well as the aforementioned automaticity (rhythmicity). It has been observed that alteration or impairment of any of these interrelated properties may result in cardiac arrhythmias. For example, A-V junctional tachycardia is an acceleration of the ectopic automaticity that may occur despite the generation of cardiac impulses at the sinus rate by the sinus node.
Excitability, which is the property of cardiac tissue to respond to a stimulus, varies with the different periods of the cardiac cycle. There is an inability of the cardiac tissue to respond to a stimulus during the portion of the refractory period termed the absolute refractory phase (approximating the interval of contraction, from the start of the QRS complex to the commencement of the T wave of the electrocardiogram), and a lower than usual response during another portion of the refractory period constituting the initial part of the relative refractory phase (coincident with the T wave). In the mid-portion of the relative refractory phase corresponding to the top of the T wave, referred to as the vulnerable period, the heart is prone to develop fibrillation in response to even a low intensity stimulus. Fibrillation is a tachyarrhythmia characterized by the commencement of completely uncoordinated random contractions by sections of conductive cardiac tissue of the affected chamber, quickly resulting in a complete loss of synchronous contraction of the overall mass of tissue and a consequent loss of the blood-pumping capability of that chamber.
Excitability of the various portions of the cardiac tissue differs according to their degree of refractoriness, with ventricular tissue being more refractory than atrial tissue and less refractory than A-V junctional tissue, for example. Similarly, the different portions of the heart vary significantly in conductivity, a related electrophysiologic property of cardiac tissue that determines the speed with which cardiac impulses are transmitted. For example, ventricular tissue is less conductive than atrial tissue and more conductive than A-V junction tissue. The longer refractory phase and slower conductivity of the A-V junctional tissue give it a significant natural protective function, which will be described presently.
Disruption of the natural pacemaking and propagation system as a result of aging or disease is commonly treated by artificial cardiac pacing, by which rhythmic electrical discharges are applied to the heart at a desired rate from the implanted artificial pacemaker (referred to throughout the remainder of this document simply as a "pacemaker"). In its simplest form, the pacemaker consists of a pulse generator powered by a self-contained battery pack, and a lead including at least one stimulating electrode electrically connected to the pulse generator. The lead is typically of the catheter type for intravenous insertion to position the stimulating electrode(s) for delivery of electrical impulses to excitable myocardial tissue in the appropriate chamber(s) in the right side of the patient's heart. However, in some instances epicardial electrodes are implanted by surgically splitting the patient's chest or other well known techniques, and suturing or screwing them in to the epicardium. Typically, the pulse generator is surgically implanted in a subcutaneous pouch in the patient's chest. In operation, the electrical stimuli are delivered to the excitable cardiac tissue via an electrical circuit that includes the stimulating and reference electrodes, and the body tissue and fluids.
A pacemaker operates in one of three different response modes, namely, asynchronous (fixed rate), inhibited (stimulus generated in absence of specified cardiac activity), or triggered (stimulus delivered in response to specified cardiac activity). The demand ventricular pacemaker, so termed because it operates only on demand, has been the most widely used type. It senses the patient's natural heart rate and applies stimuli only during periods when that rate falls below the preset pacing rate.
Pacemakers range from the simple fixed rate device that provides pacing with no sensing function, to the highly complex model implemented to provide fully automatic dual chamber pacing and sensing functions. The latter type of pacemaker is the latest in a progression toward physiologic pacing, that is, the mode of artificial pacing that restores cardiac function as much as possible toward natural pacing.
Historically, pacemakers have been employed primarily for the treatment of bradyarrhythmias, but over the past several years cardiac pacing has found significantly increasing usage in the management of tachyarrhythmias. Anti-tachyarrhythmia pacemakers take advantage of the aforementioned inhibitory mechanism that acts on the secondary natural pacemakers to prevent their spontaneous automaticity, sometimes termed "postdrive inhibition" or "overdrive inhibition". In essence, the heart may be driven (stimulated) with a faster than normal pacing rate to suppress ectopic activity in the form of premature atrial or ventricular contractions (extrasystoles) that might otherwise initiate supraventricular or ventricular tachycardia, flutter (typically, a tachyarrhythmia exceeding 200 bpm), or fibrillation; or to terminate an existing tachyarrhythmia. It should be noted that premature ventricular contractions (PVCs) may be observed in persons without evidence of heart disease.
The pulses delivered to the heart for pacing therapy need only be of sufficient magnitude to stimulate the excitable myocardial tissue in the immediate vicinity of the pacing electrode. In contrast, another technique for terminating tachycardias, termed cardioversion, utilizes apparatus to shock the heart with one or more current or voltage pulses of generally considerably higher energy content than is delivered in pacing pulses. Whether pacing or cardioverting therapy is employed in an effort to terminate a tachycardia, a considerable risk is present that the treatment itself may precipitate fibrillation.
Defibrillation ("DF"), the method employed to terminate fibrillation, involves applying one or more high energy "countershocks" to the heart in an effort to overwhelm the chaotic contractions of individual tissue sections, allow reestablishment of an organized spreading of action potential from cell to cell of the myocardium, and thus restore the synchronized contraction of the mass of tissue. The term "cardioversion" is sometimes used broadly to include DF, but in the present document, a distinction is maintained between the two terms and the techniques designated by them. In the great majority of cases, atrial fibrillation ("AF") is hemodynamically tolerated and not life-threatening because the atria provide only a relatively small portion (typically on the order of 15 to 20 percent) of the total cardiac output, i.e., the volume of blood pumped by the heart per unit time. Indeed, a technique frequently used in the past for terminating atrial flutter involves stimulating the atrium with artificial pacing pulses delivered at a rate higher than the flutter rate to convert the flutter to fibrillation. Within a relatively brief interval following cessation of the pacing, the heart usually reverts to normal sinus rhythm on its own. During this time, the tissue remains healthy because it is continuing to receive a fresh supply of oxygenated blood as a result of the continued pumping action of the ventricles.
Atrial tachycardia ("AT") may also be hemodynamically tolerated because of the aforementioned natural protective property of the A-V junctional tissue (sometimes referred to as "functional A-V block") attributable to its longer refractory period and slower conductivity than atrial tissue. This property renders the A-V junctional tissue tissue unable to fully respond to the more rapid atrial contractions. As a result, the ventricle may miss every other or perhaps two of every three contractions in the high rate atrial sequence, resulting in 2:1 or 3:1 A-V conduction, and thus maintain relatively strong cardiac output and near-normal rhythm.
Nevertheless, in cases where the patient is symptomatic or at high risk in events of AT or AF--for example, instances where the patient suffers from ventricular heart disease and consequent reduction of ventricular pumping capability, with a correspondingly greater contribution by the atria to cardiac output--special treatment of these atrial disorders is necessitated. The methods of treatment commonly prescribed by the physician include medication, drugs, pacing therapy, cardiac shock therapy, and in some cases, surgically creating an A-V block and implanting a ventricular pacemaker.
In contrast to AT, cardiac output is considerably diminished during an episode of ventricular tachycardia ("VT") because the main pumping chambers of the heart, the ventricles, are only partially filled between the rapid contractions of those chambers. Moreover, VT presents a significant risk of acceleration of the arrhythmia into ventricular fibrillation ("VF"), either spontaneously or in response to treatment of the VT. As in the case AF, ventricular fibrillation ("VF") is characterized by rapid, chaotic electrical and mechanical activity of the excitable myocardial tissue, but in contrast to AF, VF manifests an instantaneous cessation of cardiac output as the result of the ineffectual quivering of the ventricles. Unless cardiac output is restored almost immediately after the onset of VF, tissue begins to die for lack of oxygenated blood, and death will occur within minutes.
Accordingly, it is a further object of the present invention to provide an improved medical device for treating ventricular tachyarrhythmias, including ventricular tachycardia, flutter, and fibrillation, with improved techniques for detecting the arrhythmia and for distinguishing it from normal high rates, and using a hierarchical approach to the aggressiveness and delivery of therapies.
The pulse energy requirements for cardioversion and defibrillation overlap to an extent, ranging from as low as about 0.05 joule to approximately 10 joules for cardioversion and from about 5 joules to approximately 40 joules for DF. The energy level required differs from patient to patient, and depends on type of pulse waveform and electrode configuration used, as well as various other known factors.
Traditionally, practical defibrillators have been characterized by rather bulky electrical apparatus for applying a high-energy pulse through the heart via paddles placed at predetermined locations on the patient's thorax. Over the past several years, however, implantable cardioverters and defibrillators have been proposed for use in detecting and treating VT and/or VF. In 1970, M. Mirowski et al. and J. C. Schuder et al. separately reported in the scientific literature their independent proposals of a "standby automatic defibrillator" and a "completely implanted defibrillator", respectively, and experimental results in dog tests. Since that time, a vast number of improvements in implantable cardioverters and defibrillators, including electrode placement using extrapericardial patches or transvenous catheters, has been reported in the scientific literature and patent publications. A fairly representative sampling is as follows:
U.S. Pat. No. 3,805,795 issued Apr. 23, 1974 to Denniston et al. describes a defibrillator circuit with implanted electrodes for delivering defibrillating pulses to the heart only if separate signals respectively indicative of electrical and mechanical activity are both absent for a predetermined period of time, and in which the first pulse delivered is of lower energy content than succeeding pulses.
U.S. Pat. No. 4,114,628 issued Sept. 19, 1978 to Rizk describes a demand pacemaker with an automatically adjusted threshold, and having an operating mode in which a difibrillating pulse is automatically applied to the patient's heart in the absence of cardiac activity for a predetermined period of time.
U.S. Pat. No. Re. 27,652 to Mirowski et al. describes an automatic implantable defibrillator in which a preset delay is imposed between successive shocks, and in which further shocks are inhibited following successful defibrillation.
U.S. Pat. No. 4,181,133 issued Jan. 1, 1980 to Kolenik et al. describes a programmable implantable pacemaker which provides the dual functions of demand pacing and standby cardioversion of tachycardias. U.S. Pat. No. 4,300,567 issued Nov. 17, 1981 to Kolenik et al. describes an implantable automatic defibrillator adapted to deliver a high energy defibrillating pulse in one mode and lower energy cardioverting pulses in another mode.
Generally speaking, the implantable defibrillators of the prior art detect ECG changes and/or absence of a "mechanical" function such as rhythmic contractions, pulsatile arterial pressure, or respiration, and in response deliver a fixed therapy typically consisting of one or more shocking pulses of preset waveform and energy content. If any other cardiac therapy is available from the device, such as cardioversion for treatment of tachycardia, it too is delivered according to a fixed plan in response to conventional detection of the specific arrhythmia. While many of these proposed devices appear to be capable of functioning as they are described in the literature, and may become widely available in the future, they offer little or no flexibility of therapy regimen or capability to detect subtle changes in the arrhythmia to be treated and to respond with appropriate therapy.
Accordingly, it is another general object of the present invention to provide an implantable cardiac stimulator adapted to arrest a detected arrhythmia by selectively delivering any of a plurality of sequences of dissimilar therapies depending on the degree of hemodynamic tolerance (or intolerance) of the patient to the detected arrhythmia.
A related object of the invention is to provide such an implantable cardiac stimulator further adapted to detect a change in the arrhythmia and to respond thereto by selective delivery of a therapy sequence which may be more or less aggressive (in terms of likelihood of arresting the arrhythmia) than the immediately preceding therapy sequence, depending on direction and extent of the arrhythmia change.
In copending U.S. patent application Ser. No. 765,047, filed Aug. 12, 1985 (hereinafter referred to as "the 765,047 application"), assigned to the same assignee as is the present invention, an antitachycardia pacemaker is disclosed in which a microprocessor is programmed to detect pace-terminable tachycardias, such as reentrant tachycardias (i.e., tachycardias characterized by a premature beat and constant coupling interval because of localized refractoriness), using a detection algorithm which selectively includes high rate, rate stability, sudden onset and sustained high rate tests. When a tachycardia is detected, the pacemaker responds in a programmed fashion toward terminating the tachycardia by applying programmed bursts of stimulating pulses to the heart in accordance with selected treatment modalities. If a detected tachycardia is similar to a previous successfully terminated tachycardia, the pacemaker programming will re-apply the previous successful treatment modality in an initial attempt to terminate the new tachycardia. The start delay and pulse-to-pulse interval may be defined as fixed program values, or as adaptive values derived as a percentage of the detected high rate interval. If a burst is generated, the start delay of the burst or the pulse-to-pulse interval of the burst may be scanned by incrementing or decrementing the values of these parameters a preseleceted number of steps or by incrementing and decrementing the parameters in a predefined search pattern. Alternatively, the intervals of the pulses within a burst are automatically decremented in the autodecremental mode.
The antitachycardia pacemaker of the 765,047 application represents a distinct and significant improvement over previous devices of that general type, in such aspects as the nature of the detection system, techniques for distinguishing pace-terminable tachycardias from other tachycardias, and application of pacing therapies toward extinguishing such detected pace-terminable tachycardias. However, that device is somewhat one-dimensional in its detection and treatment capabilities, to a great extent being restricted to pace-terminable atrial tachycardias and pacing therapies, although it serves that medical application quite well.
Therefore, a more specific object of the present invention is to provide an improved implantable medical device adapted to detect ventricular tachycardias and other arrhythmias throughout the heart rate continuum, and automatically responsive to such detection to selectively deliver one or more of a plurality of predetermined therapies, including bradycardia and antitachycardia pacing-type therapies and cardioverting and DF shock-type therapies, in different regimens of dissimilar aggressiveness of treatment according to the degree of hemodynamic tolerance or intolerance of the detected arrhythmia.
Antitachycardia pacemakers are typically utilized against atrial tachycardia, and are generally unsuitable for treating VT because of the risk of accelerating the latter to VF and the inability of such devices to respond effectively to the acceleration.
Accordingly, another object of the invention is to provide a medical device suitable for delivering antitachycardia pacing therapy for managing ventricular tachycardias, and having additional or backup capabilities for terminating VF in the event of acceleration, and thereby to lessen the risk associated with using pacing therapies to treat VT.